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Hyperhomocysteinemia and arteriosclerosis: historical perspectives
1Pathology and Laboratory Medicine Service, Veterans Affairs Medical Center, West Roxbury, MA 02132, USA. Kilmer.mccully@med.va.gov
Clinical Chemistry and Laboratory Medicine
|October 4, 2005
Summary
Elevated homocysteine is a key risk factor for arteriosclerosis. Research links this amino acid to arterial damage, supporting the homocysteine theory of this vascular disease.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Pathology
Background:
- Arteriosclerosis origins were explored in the 19th century, with early theories focusing on inflammation and lipid deposition.
- Experimental studies in the early 20th century linked dietary factors like protein and cholesterol to arteriosclerosis in animals.
Observation:
- Deficiencies in enzymes related to methionine metabolism, such as cystathionine synthase and methionine synthase, were found to cause thrombosis and vascular disease.
- McCully's 1969 findings in methionine synthase deficiency (cobalamin C disease) directly linked arteriosclerosis to metabolic issues.
Findings:
- The homocysteine theory explains experimental arteriosclerosis through deficiencies in nutrients like vitamin B6, choline, and methionine.
- Homocysteine demonstrated thrombogenic and atherogenic effects in animal models, mirroring human pathological findings.
- Elevated plasma homocysteine is now recognized as a significant independent risk factor for arteriosclerosis in the general population.
Implications:
- This research validates the homocysteine theory of arteriosclerosis.
- Understanding homocysteine's role opens avenues for new diagnostic and therapeutic strategies for vascular disease prevention and treatment.